Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunoreactive gamma-glutamyl transpeptidase in human serum and liver tissue was measured by a solid phase enzyme-linked immunosorbent assay. The immunoreactive gamma-glutamyl transpeptidase was significantly elevated in the sera of patient with hepatocellular carcinoma. On the other hand, in sera of patients with non-neoplastic diseases, including chronic hepatitis, acute hepatitis, fatty liver and hemangioma, the immunoreactive gamma-glutamyl transpeptidase was not elevated. In hepatocellular carcinoma and metastatic liver tumor tissues, the immunoreactive gamma-glutamyl transpeptidase content was also elevated, showing good correlation with the enzyme protein content in sera. However, no correlation was found between the activity of gamma-glutamyl transpeptidase determined by an enzymatic assay and the content determined by an enzyme-linked immunosorbent assay. On immunohistochemical examination, the immunoreactive enzyme protein without enzymatic activity was detected only in the cytoplasm of cancer cells. This suggested that there is an increased level of the immunologically active but enzymatically inactive form of gamma-glutamyl transpeptidase in hepatoma tissues.
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PMID:Measurement of immunoreactive gamma-glutamyl transpeptidase in human sera and liver tissues of patients with various liver diseases. 257 Jul 27

From June, 1969 to February, 1987, distal splenorenal shunt was carried out on 78 patients with esophagogastric varices. The operations were urgent in 9, elective in 40, and prophylactic in 29 patients. There were 52 males and 26 females. Age ranged from 16 to 76 years with an average of 53 years. Thirty-seven patients were alcoholics. Hepatitis B surface antigen was positive in only 15.5%. The causes of portal hypertension were cirrhosis of the liver in 67, chronic hepatitis in 5, idiopathic portal hypertension in 4, primary biliary cirrhosis in 1, and fatty liver in 1 patient. Fifty-two patients were in Child's class A, 18 in class B, and 8 in class C. Emergency shunts were performed only when conservative therapy had failed to stop variceal bleeding. Prophylactic operations were done in patients having Child's class A or class B liver disease and risky varices, in varices larger than 5 mm in diameter and/or varices with red color signs such as cherry red spots. Forty-two patients underwent the original Warren shunt, but the remaining 36 had modified distal splenorenal shunt with expanded polytetrafluoroethylene interposition. The operative mortality rates were 11.1% in the emergency group, 2.5% in the elective group, and 3.4% in the prophylactic group. The overall operative and hospital death rates were 3.8% and 7.7%, respectively. The patency rate was 94.1% and the incidence of rebleeding from esophageal varices was 3.8%. Hepatic encephalopathy, although mild to moderate in degree, was observed in 14.7% of 75 patients excluding 3 operative deaths.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Appraisal of distal splenorenal shunt in the treatment of esophageal varices: an analysis of prophylactic, emergency, and elective shunts. 278 85

Certain behaviors can have an influence on the cause and progression of liver disorders. To clarify the relation between histopathological change of the liver and psychosocial stress, behavioral traits, and psychological state, patients with fatty liver (n = 14) were compared with patients with chronic hepatitis (n = 16). Both groups were alcohol-induced without other causes and consumed the same dose of alcohol. By morphometric methods, fat deposit ratio (FDR) and degree of liver damage (DLD) which reflects lobular fibrosis, inflammatory cell infiltration, and necrosis were evaluated. Life Change Unit scores from the Social Readjustment Rating Scale were significantly higher in chronic hepatitis than in fatty liver (p less than 0.001). DLD was significantly correlated with Life Change Unit (r = 0.59, p less than 0.01). It is suggested that psychosocial stress is one of the aggravating factors of fibrosis and inflammatory change of the liver which is previously damaged by alcohol in man just like the rat liver following stress.
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PMID:Impact of stress on alcoholic liver injury; a histopathological study. 279 24

Purpose of this study was to elucidate the difference in severity of alcoholic liver diseases (ALD), especially of alcoholic hepatitis (AH) between female and male. We have experienced 15 female and 113 male patients with ALD laparoscopically and histologically proved during the past 10 years. In female patients, histological analysis revealed 8 cases of cirrhosis, 2 each cases of AH, fibrosis and chronic hepatitis, and 1 case of fatty liver. Occurrence of AH in female (13%) was significantly higher than male in which AH was seen in 3 cases (3%) (p less than 0.05). Duration of alcoholic abuse in female AH patients was shorter than male AH patients (5.5 +/- 0.5 years vs 24.0 +/- 2.9 years). Total alcohol consumed in female AH patients was less than male AH patients (256 +/- 52 kg vs 1560 +/- 703 kg). Abnormality in liver function tests including hepaplastin test, serum bilirubin, transaminases, lactate dehydrogenase, alkaline phosphatase, gamma-glutamyltranspeptidase, immunoglobulins was outstanding in female patients compared with male patients. Histological findings such as hepatocellular ballooning, neutrophilic infiltration, fatty change and wiremesh fibrosis were intensive in female patients compared with male patients. In conclusion, there were much more severe ALD like AH or cirrhosis in female than male patients. In female AH patients duration of alcoholic abuse was shorter and total alcohol consumed was less than male AH patients. And it was suggested that female AH is clinically and pathologically getting severe compared with male AH.
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PMID:[Sex difference in alcoholic liver disease: with special reference to the severity of alcoholic hepatitis]. 280 7

A solid phase enzyme-linked immunosorbent assay for human immunoreactive gamma-glutamyltranspeptidase(gamma-GTP) was developed. The working range by this assay was from 1 ng to 100 ng. Serum immunoreactive gamma-GTP was significantly elevated in patient with hepatocellular carcinoma and moderate elevation was found in liver cirrhosis. On the other hand, in sera of patients with non neoplastic disease, including acute hepatitis, chronic hepatitis, fatty liver, hemangioma, the immunoreactive gamma-GTP was not significantly elevated. No correlation was found between the serum levels of gamma-GTP determined by enzymatic assay and enzyme-linked immunosorbent assay. In the tissues of hepatocellular carcinoma and metastatic liver tumor, the immunoreactive gamma-GTP contents were also elevated, which were well correlated with the enzyme contents in sera. When immunohistochemical study was carried out, the immunoreactive gamma-GTP was detected diffusely not only in the cell membrane and bile canaliculi but also in the cytoplasm of cancer cell. These results suggest that the hepatoma tissues contain an immunologically active, but enzymatically inactive form of gamma-GTP enzyme.
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PMID:[Measurement of human serum and liver tissue immunoreactive gamma-glutamyl transpeptidase in patients with various liver diseases]. 289 51

From these discussions, it is apparent that: Alcoholic liver disease is increasing at a rapid rate in conjunction with an increase of annual gross and per capita consumption of alcohol. Alcoholic hepatitis and alcoholic hyaline are much less common in Japan compared to western countries. Alcoholic hepatic fibrosis and chronic hepatitis are the common types of alcoholic liver disease in Japan. Alcoholic hepatic fibrosis may be a pathological process or entity independent of fatty liver, alcoholic hepatitis, and alcoholic cirrhosis. It is not clear at the present time whether heavy alcohol consumption per se or non-A, non-B hepatitis virus is the cause of chronic hepatitis seen in HBsAg negative alcoholics.
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PMID:Alcoholic liver disease in Japan. 302 74

This report presents results of studies using the spectral-shift zero-crossing method to measure frequency-dependent attenuation (FDA) in normal liver and spleen and in diseased liver. We developed a new system for attenuation analysis that calculated FDA in dB/cm/MHz according to the following equation: (formula: see text). Data are collected from the region of interest on the scan image. Graphite-gel phantoms of known attenuation value are used to create a high degree of accuracy in this new system. Mean attenuation of normal livers was 0.55 +/- 0.05 dB/cm/MHz, while that of normal spleen was 0.37 +/- 0.06 dB/cm/MHz. No correlation between FDA and age could be seen. FDA was 0.81 +/- 0.17 dB/cm/MHz in fatty liver, 0.63 +/- 0.13 dB/cm/MHz in liver cirrhosis, and 0.64 +/- 0.12 dB/cm/MHz in chronic hepatitis. These values are higher than those obtained from normal liver, while tumor masses in the liver (hepatocellular carcinoma, hepatoblastoma, hemangioma) and diffuse infiltration by malignant lymphoma produced lower than normal values, averaging 0.38 +/- 0.08 dB/cm/MHz.
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PMID:Studies on frequency-dependent attenuation in the normal liver and spleen and in liver diseases, using the spectral-shift zero-crossing method. 315 99

Serial assays for immunoglobulin M antibody to hepatitis B core antigen (IgM anti-HBc) were performed in 51 patients with antibody to hepatitis B e antigen (anti-HBe) in their sera. IgM anti-HBc was detected periodically and persistently in 8 (53%) of 15 patients with chronic hepatitis whose serum glutamic pyruvic transaminase (GPT) levels were elevated and was not detected in 36 patients with normal serum GPT levels. Antibody to delta agent was not detected in any of the patients. Of the eight patients positive for IgM anti-HBc, four had a high titer of IgM anti-HBc and either developed liver cirrhosis (three cases) or died due to massive hepatic necrosis (one case); the other four showed a low level of IgM anti-HBc and either recovered (two cases) or developed chronic persistent hepatitis (two cases). Of seven patients negative for IgM anti-Hbc, two had a fatty liver, and five, who had a history of blood transfusion, had chronic hepatitis. Thus, even though anti-HBe may be present, if the titer of IgM anti-HBc is high, the histological activity can be expected to increase, and the prognosis will be poor. If the titer of IgM anti-HBc is low, the histological activity may be expected to decrease, and the prognosis may be good. In patients with abnormally high serum GPT but without IgM anti-HBc, another type of hepatitis or a secondary form of liver disease should be considered.
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PMID:Serial assay for IGM anti-HBc in patients with anti-HBe-positive chronic hepatitis and its significance for long-term prognosis. 336 33

One-hundred-and-ten children between the ages of two months and 14 years with the following liver diseases were studied: 16 with acute viral hepatitis, 8 with persistent chronic hepatitis, 31 with active chronic hepatitis, 5 with hepatic steatosis, 11 with cirrhosis of the liver, 24 with newborn cholestasis, 3 with Wilson's disease, 2 with congenital hepatic fibrosis, 5 with metabolic diseases and 5 due to other causes. These children presented Pi system phenotypes in isoelectric focus using ultrafine polyacrylamide gels according to Kuepper's method, with modifications incorporated to determine Alpha-1-antitrypsin (A1-AT) serum level deficiencies in those presenting the Pi ZZ phenotype, a liver biopsy with P.A.S. coloration on digestion of diastase and a family history of the phenotype. Four (3.6%) of the children with Pi ZZ phenotypes showed a decrease of serum A1-AT and the presence of positive P.A.S. inclusions resistant to diastase in the cytoplasm of hepatocytes. Three had a history of postnatal icterus and the fourth presented hepatomegaly. The phenotypic study of the parents showed their being heterozygous (MZ), while siblings were normal (MM). The importance of the diagnosis of A1-AT deficiency and the diagnostic value of detecting Pi system phenotypes in every case of liver disease in children and adolescents is stressed.
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PMID:[The value of the Pi system phenotype in alpha 1-antitrypsin deficiency]. 349 88

Coexistence of hyperinsulinemia and normal or impaired carbohydrate tolerance indicates insulin resistance which is frequently observed in patients with liver diseases such as liver cirrhosis, fatty liver, acute and chronic hepatitis and idiopathic haemochromatosis. Insulin resistance in liver diseases can be due to circulating insulin antagonists or a target tissue defect in insulin action, either due to changes in the state of the insulin receptor or due to a postreceptor defect, that means any abnormality in the insulin action sequence following the initial binding step. High insulin levels in liver diseases are caused by diminished degradation of insulin by the liver whereas hypersecretion only plays a minor role under basal conditions. High levels of glucagon, free fatty acids and growth hormone are well known in liver diseases but until now there is no evidence of the pathogenetic importance of these factors. Conflicting results on insulin binding, methodological criticism on binding data and the question whether or not diminished insulin binding on peripheral blood cells plays any physiological role make it unlikely that studies on insulin receptors of peripheral blood cells contribute to the revelation of insulin resistance in liver diseases. The clamp technique allows to quantify the sensitivity of the body to exogenous insulin. The results on liver cirrhosis in connection with studies on glucose metabolism show that under basal conditions insulin insensitivity is due to peripheral resistance (primarily muscle) according to a postreceptor defect. Finally the causes of insulin resistance in liver diseases are still not known.
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PMID:[Insulin resistance in liver diseases]. 353 94


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